Related Experiment Video

Updated: May 13, 2026

Genetic Profiling and Genome-Scale Dropout Screening to Identify Therapeutic Targets in Mouse Models of Malignant Peripheral Nerve Sheath Tumor
09:33

Genetic Profiling and Genome-Scale Dropout Screening to Identify Therapeutic Targets in Mouse Models of Malignant Peripheral Nerve Sheath Tumor

Published on: August 25, 2023

SMO and AKT1 mutations occur in non-NF2 meningiomas

    Cancer Discovery
    |March 12, 2013
    PubMed

    Insights

    Recurrent mutations in SMO and AKT1 genes are not found together with NF2 loss in meningioma tumors. This finding clarifies the genetic landscape of meningioma, aiding in understanding tumor development.

    Area of Science:

    • Neuro-oncology
    • Cancer Genomics

    Background:

    • Meningioma is a common primary brain tumor.
    • Understanding the genetic drivers of meningioma is crucial for developing targeted therapies.

    Discussion:

    • Investigated the interplay between mutations in SMO, AKT1, and NF2 loss in meningioma.
    • Found that SMO and AKT1 mutations are mutually exclusive events with NF2 loss.

    Key Insights:

    • Recurrent SMO mutations and AKT1 mutations do not co-occur with NF2 loss in meningioma.
    • This mutual exclusivity suggests distinct molecular pathways driving meningioma subtypes.

    Outlook:

    • Further research into these distinct pathways may reveal new therapeutic targets.
    • Understanding these genetic interactions can improve meningioma classification and treatment strategies.

    More Related Videos

    Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models08:57

    Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

    Published on: May 17, 2024

    Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells09:37

    Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

    Published on: August 25, 2021

    Related Concept Videos

    mTOR Signaling and Cancer Progression03:03

    mTOR Signaling and Cancer Progression

    The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
    The mTOR pathway or the...
    Loss of Tumor Suppressor Gene Functions01:12

    Loss of Tumor Suppressor Gene Functions

    Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
    When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
    PI3K/mTOR/AKT Signaling Pathway01:22

    PI3K/mTOR/AKT Signaling Pathway

    The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
    Abnormal Proliferation02:23

    Abnormal Proliferation

    Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
    The Ras Gene02:38

    The Ras Gene

    The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
    Ras is a superfamily...
    Cancers Originate from Somatic Mutations in a Single Cell02:21

    Cancers Originate from Somatic Mutations in a Single Cell

    Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...